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March 1976

Sequelae of Carbon Monoxide-Induced Hypoxia in the Rat

Author Affiliations

From the Department of Neurology (Drs Petajan, Packham, and Frens), the Flammability Research Center (Drs Petajan and Packham and Mr Dinger), and the Department of Physiology (Mr Dinger), University of Utah colleges of medicine and engineering, Salt Lake City.

Arch Neurol. 1976;33(3):152-157. doi:10.1001/archneur.1976.00500030008002

• Rats were exposed to carbon monoxide, and conduction velocity of ventral caudal nerve (VCN), visual cortical evoked potential (VEP), electroencephalogram, and vital functions were determined in relation to the degree of CO-induced hypoxia. The conduction velocity of VCN and VEP (latency of P2 [second positive deflection of the visual evoked response]) were unaffected until carboxyhemoglobin (COHb) levels reached between 60% and 70%. These levels were maintained for approximately one hour before decreased conduction velocity or increased latency of P2 occurred. Decrease in mean arterial blood pressure resulted in impaired neurological function. Recovery of conduction velocity was discontinuous. Conduction was lost and recovered again within a three-hour period after exposure. It decreased again 9 to 13 days later, recovering in approximately four days. Data on P2 latency after exposure were fragmentary, but suggest that later increases might occur. Similar effects of CO-induced hypoxia on peripheral and central nervous systems were found. Decrease of mean arterial blood pressure was consistently associated with impaired nervous system function.